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• W2893152684 abstract "Abstract Transmigration and activation of neutrophils in the lung reflect key steps in the progression of acute lung injury (ALI). It is known that hydrogen sulfide (H 2 S) can limit neutrophil activation, but the respective mechanisms remain elusive. Here, we aimed to examine the underlying pathways in pulmonary inflammation. In vivo , C57BL/6N mice received the H 2 S slow releasing compound GYY4137 prior to lipopolysaccharide (LPS) inhalation. LPS challenge led to pulmonary injury, inflammation, and neutrophil transmigration that were inhibited in response to H 2 S pretreatment. Moreover, H 2 S reduced mRNA expression of macrophage inflammatory protein-2 (MIP-2) and its receptor in lung tissue, as well as the accumulation of MIP-2 and interleukin-1β in the alveolar space. In vitro , GYY4137 did not exert toxic effects on Hoxb8 neutrophils, but prevented their transmigration through an endothelial barrier in the presence and absence of MIP-2. In addition, the release of MIP-2 and reactive oxygen species from LPS-stimulated Hoxb8 neutrophils were directly inhibited by H 2 S. Taken together, we provide first evidence that H 2 S limits lung neutrophil sequestration upon LPS challenge. As proposed underlying mechanisms, H 2 S prevents neutrophil transmigration through the inflamed endothelium and directly inhibits pro-inflammatory as well as oxidative signalling in neutrophils. Subsequently, H 2 S pretreatment ameliorates LPS-induced ALI." @default.
• W2893152684 created "2018-10-05" @default.
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• W2893152684 date "2018-10-02" @default.
• W2893152684 modified "2023-10-10" @default.
• W2893152684 title "Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury" @default.
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• W2893152684 doi "https://doi.org/10.1038/s41598-018-33101-x" @default.
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